Mladenova Irena
Department of Hygiene, Epidemiology and Infectious Diseases, Faculty of Medicine, Trakia University, Stara Zagora, Bulgaria -
Minerva Cardioangiol. 2019 Oct;67(5):425-432. doi: 10.23736/S0026-4725.19.04986-7. Epub 2019 Jul 24.
Many studies have been performed concerning the potential role of Helicobacter pylori (H. pylori) in different extra-gastric diseases. Ischemic heart disease (IHD) remains the leading cause of mortality in developed countries. The traditional cardiovascular risk factors could not predict all cases of IHD. Hence, the scientists explore other potential etiologic factors, especially infections. H. pylori infection has been suspected to have a role in the pathogenesis of atherosclerosis. However, after 25 years from the first description, the role of the bacterium in the pathogenesis of IHD remains controversial and enigmatic. Since H. pylori infection is persistent and stimulates both a local and a systemic immune response that could cause significant changes in the markers of inflammation like cytokines, C-reactive protein, heat shock protein, fibrinogen, triglycerides, high density lipoprotein, it has been supposed that the outcomes of this process are atherosclerosis and a prothrombotic state which eventually leads to IHD. Alternative pathogenic mechanisms have been hypothesized, including the occurrence of molecular antigenicity. This hypothesis supposed that H. pylori could provoke autoimmunity as a result of molecular mimicry. The eradication of H. pylori infection as cardiovascular prevention strategy has been the object of some studies. However, the results are of difficult interpretation. Further studies, especially with a cohort and interventional design, have to be performed to reveal the potential relationship between H. pylori and IHD.
关于幽门螺杆菌(H. pylori)在不同胃外疾病中的潜在作用,已经开展了许多研究。缺血性心脏病(IHD)仍然是发达国家的主要死因。传统的心血管危险因素无法预测所有IHD病例。因此,科学家们探索其他潜在的病因,尤其是感染因素。幽门螺杆菌感染被怀疑在动脉粥样硬化的发病机制中起作用。然而,自首次描述以来的25年里,这种细菌在IHD发病机制中的作用仍然存在争议且难以捉摸。由于幽门螺杆菌感染具有持续性,并刺激局部和全身免疫反应,这可能导致炎症标志物如细胞因子、C反应蛋白、热休克蛋白、纤维蛋白原、甘油三酯、高密度脂蛋白发生显著变化,因此人们推测这个过程的结果是动脉粥样硬化和血栓前状态,最终导致IHD。也有人提出了其他致病机制,包括分子抗原性的出现。该假说认为幽门螺杆菌可能由于分子模拟而引发自身免疫。将根除幽门螺杆菌感染作为心血管预防策略一直是一些研究的对象。然而,结果难以解释。必须开展进一步的研究,尤其是队列研究和干预性设计研究,以揭示幽门螺杆菌与IHD之间的潜在关系。